BACKGROUND: The role of oxidative stress in inflammatory bowel diseases (IBD) has been extended lately from a simple consequence of inflammation to a potential etiological factor, but the data are still controversial. Active disease has been characterized before by an enhanced production of reactive oxygen species and the increased peroxidation of lipids, but patients in remission were generally not considered different from healthy people in terms of oxidative stress. AIMS: We evaluated the antioxidant defense capacity and lipid peroxidation status in the serum of patients with active and non-active disease compared with healthy matched control subjects. METHODS: The study included 20 patients with confirmed IBD in clinical and biological remission, 21 patients with active disease, and 18 controls. We determined the serum levels of two antioxidant enzymes, superoxide dismutase (SOD) and glutathione peroxidase (GPX), and a lipid peroxidation marker, malondialdehyde (MDA). RESULTS: Active disease patients had an increased activity of both SOD and GPX, as well as significant high values of MDA versus controls. Furthermore, patients being in remission had significantly lower values of antioxidant enzymes (SOD and GPX) and increased lipid peroxidation measured by MDA serum levels, as compared with healthy control subjects. CONCLUSIONS: Our study confirmed the presence of high oxidative stress in active IBD. More importantly, we have demonstrated a lower antioxidant capacity of patients in remission versus control group. This may represent a risk factor for the disease and can be an additional argument for the direct implication of oxidative stress in the pathogenesis of IBD.
BACKGROUND: The role of oxidative stress in inflammatory bowel diseases (IBD) has been extended lately from a simple consequence of inflammation to a potential etiological factor, but the data are still controversial. Active disease has been characterized before by an enhanced production of reactive oxygen species and the increased peroxidation of lipids, but patients in remission were generally not considered different from healthy people in terms of oxidative stress. AIMS: We evaluated the antioxidant defense capacity and lipid peroxidation status in the serum of patients with active and non-active disease compared with healthy matched control subjects. METHODS: The study included 20 patients with confirmed IBD in clinical and biological remission, 21 patients with active disease, and 18 controls. We determined the serum levels of two antioxidant enzymes, superoxide dismutase (SOD) and glutathione peroxidase (GPX), and a lipid peroxidation marker, malondialdehyde (MDA). RESULTS:Active diseasepatients had an increased activity of both SOD and GPX, as well as significant high values of MDA versus controls. Furthermore, patients being in remission had significantly lower values of antioxidant enzymes (SOD and GPX) and increased lipid peroxidation measured by MDA serum levels, as compared with healthy control subjects. CONCLUSIONS: Our study confirmed the presence of high oxidative stress in active IBD. More importantly, we have demonstrated a lower antioxidant capacity of patients in remission versus control group. This may represent a risk factor for the disease and can be an additional argument for the direct implication of oxidative stress in the pathogenesis of IBD.
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